The genes of the mitochondrion (kinetoplast) of some Kinetoplastida - e.g. Trypanosoma brucei, the parasite which causes African sleeping sickness - are "encoded" in a way that the pre mRNA requiries partially heavy editing (insertion and deletion of Uridines) by the editosome (a RNA/Protein complex) until it can be translated to the correct proteins. The information where to insert and remove Uridines is contained in small gRNA also part of the mitochondrial genome.

However this whole thing seems kind of unnecessary to me. Why did evolution not get rid of the surplus/missing Thymidines in those Genes? What's the use of this?

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    $\begingroup$ Parsimony is not the prevailing paradigm of biology - rather it might be opacity $\endgroup$ – shigeta Feb 2 '14 at 17:11

You could have asked a similar question about splicing. The function of RNA editing seems to be similar: it's one of the ways to trigger production of alternative transcripts and proteins given the same DNA sequence.

The question is discussed, for example, in this review. The authors describe different known effects of alternative RNA editing:

  • Amino-acid substitutions
  • ORF extension
  • New unique ORFs
  • Alternative UTRs

Alternative editing is correlated with developmental stage, which is not surprising, given the fact that the parasites switch their energy metabolism in different hosts (1,2,3), with the mitochondria changing their structure accordingly.

The authors seem to be astonished as well and conclude: "RNA editing in kinetoplastid mitochondria is a beautiful example how evolution favors diversifying mechanisms even if they seem to be extremely wasteful from a human perspective."

  • $\begingroup$ Haha, I read that last quote just the second before I read your answer. I find this answer much more satisfying than the neutral model proposed in 10.1016/0168-9525(93)90011-6. I like how you point out the different oxygen concentrations[source would be nice] as one would usually think of the mitochondrial genes as almost perfect and thus less variable. However, some (healthy?) doubt is left... $\endgroup$ – jan-glx Feb 2 '14 at 18:31
  • $\begingroup$ I've replaced the oxygen part of the answer with a more cautious and correct phrase. Sources are provided :) $\endgroup$ – har-wradim Feb 3 '14 at 12:05
  • $\begingroup$ One important point in my opinion, which opposes the neutrality hypothesis is that the minimal number of gRNAs potentially required for RNA editing (~150) is much less than the observed variability (~1000) (see p. 230), which again hints at adjustability of the system and at the biological relevance of this adjustability. $\endgroup$ – har-wradim Feb 3 '14 at 12:17
  • $\begingroup$ Thanks! I kinda agree on that last point through I don't think that this really challenges the neutral hypothesis ("see we have 850 neutral gRNA developed by chance. Now if a mutation in a gene occurs that can be rescued by one of those gRNA this change will also be neutral but will lead to a fixation of that gRNA"). Is Neutrality even the basis of diversity and thus adjustability?(and thus not neutral, hah) $\endgroup$ – jan-glx Feb 6 '14 at 13:09
  • $\begingroup$ If in this system a new gRNA emerges and gains no function in the nearest future, its destiny is to be lost within several generations. It's like a plasmid in bacteria: if you don't create a selective pressure (e.g., antibiotic with its respective antidote coded by the plasmid), the plasmid is quickly lost. And in this case we have a large pool of gRNAs, which are at first glance redundant. $\endgroup$ – har-wradim Feb 6 '14 at 22:31

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